Abstract
The degree of methionine overproduction by metK mutants defective in S-adenosylmethionine (SAM) synthetase is shown to reflect, with one exception, the loss of function of this enzyme thus giving further support to the hypothesis that SAM is the co-repressor of this system. The exceptional mutant (metKx721) has a high constitutive SAM synthetase activity but its methionine production resembles that of mutants with no measurable SAM synthetase activity (typical metKx mutants) and this and other properties of the mutant suggest that the wild-type SAM synthetase protein has a role in methionine repression. Methionine repression control does not extend to the enzymes of spermidine synthesis from SAM but metKx mutants have a higher rate of utilization of SAM by this pathway than wild-type or other regulatory mutants. This could mean that the wild-type SAM synthetase molecule interacts with an enzyme of this pathway thus lowering its activity.
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